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Clin Med III > Exam 2 CM3 PUD > Flashcards

Exam 2 CM3 PUD Flashcards

1
Q

PUD def? Prevalence? Who is affected?

A

Ulcers that may occur in Distal esophagus, stomach or duodenum
10% ED pt with abd pain are PUD dx
Low prevalence in US bc Eradication of H pylori, but increasing in developing countries
M:F 1:2; increases with age

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2
Q

Where does PUD occur? Risk factors?

A

In areas of GI tract exposed to acid and pepsin duodenal bulb and stomach commonly
Risks
H pylori (>90% duodenal ulcers, up to 70% gastric)
NSAIDS: esp gastric ulcers
Hypersecretory states (ZES)
Smoking (relation with ETOH, spicy food, stress)

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3
Q

What is H pylori and how do you get it

A

G- rod with 6 motile flagellum that enable it to attach to mucosa; presumed to disrupt protective properties by decreasing gastric mucus and mucosal bicarb secretion
Genetic predisposition
Transmitted and colonized as children (oral/oral or fecal/oral)
Infection = chronic UNELSS treated with abx

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4
Q

How does H pylori affect the GI tract

A

Causes change in gastric pH and gastric acid secretion (secretion increases 6 fold)
duodenal mucosal bicarb secretion
gastric mucus content

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5
Q

How are NSAIDS related to ulcers and how do they affect the gastric mucosa

A

15-20% CHRONIC NSAID users duodenal ulcers (bc inhibit Prostaglandins)
Increased with age, F, dose, long term NSAID use, severe co-morbidities
Disruption of mucosal defenses by both topical and systemic effects (gastric more freq than duodenal)

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6
Q

Topical effects of NSAIDS include

A

Mostly in stomach, may result from direct toxic insult on gastric mucosa
*NSAIDS diffuse freely across the mucosal barrier cause cytotoxicity (See submucosal hemorrhages and erosions with grow bleeding
NSAIDS may alter local immune response (direct leukocytes against the gastric mucosa; local inhibition of COX)

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7
Q

How do NSAIDS cause systemic effects

A

Inhibit COX enzyme in gastric epithelium to decrease PG production

  • diminished PGs alter defensive properties of gastroduodenal mucosa
  • Acid and pepsin cause more mucosal damage leading to ulcers
  • Gastric mucosal barrier even more vulnerable to normal gastric secretions

*even enteric coated or IV NSAIDS can cause ulcers through systemic effects

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8
Q

What is dyspepsia and what causes it

A

Chronic and recurrent upper abd discomfort (indigestion).

  • unclear pathopys: assoc with delayed gastric emptying, gastric hypersensitivity, H pylori
  • sx: chronic & intermittent; post prandial fullness and bloating
  • also epigastric pain, early satiety, N, belching

alarm sx: wt loss, recurrent vomiting, bleeding, anemia, dysphagia, jaundice, palpable mass

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9
Q

How do you dx Dyspepsia

A

Generally: test and treat

  • UGI or Endoscopy are the gold standards
  • initial testing should r/o H.pylori (if neg for H pylori, can treat pt with anti secretory or prokinetic meds (ie Reglan)
  • diet: freq small meals, low fat
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10
Q

What would the typical hx of a pt with PUD be

A

Present: mid epigastric abd pain, may radiate to back

  • Burning, gnawing, boring (change in character of pain suggests complications)
  • Bloating belching possible
  • May see anemia sx ie fatigue and dyspnea
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11
Q

Contrast Duodenal v Gastric ulcers

A

Duodenal: episodic, pain 2-3hr post eating, wakes them up at night, relieved by eating or antacids, uncommon to see N/V wt loss

Gastric: continuous pain, worse after eating (w/in 30min), antacids not helpful, may se N/V, wt loss

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12
Q

PE findings of PUD

A

Mild epigastric tenderness
BS normal
*Perform rectal exam with guaiac to r/o bleeding
*If obstruction: see abd distension, High pitched BS [supine and upright film, air fluid levels]
*if perforated: abdominal rigidity and guarding, rebound tenderness [look for free air under diaphram on upright abd film]

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13
Q

Ddx PUD

A

ACS, AA, GERD/esophagitis, gastroenteritis, pancreatitis, pancreatic CA, PE, renal calculi, gastric CA, atrophic gastritis, mesenteric ischemia, functional GI disorder

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14
Q

How do you dx PUD

A

Blood tests generally unhelpful, but get CBC to r/o anemia

Urea breath tests: carbon radio labeled urea, collect breath sample 10-20 min later, analyze for CO2 (high sens/spec) (can be altered in pt on PPI or abx)

  • Serologic tests for IgG & H pylori antibodies indicate prior exposure, not current infection
  • Bacterial cultures, somewhat sensitive, 100% specific
  • stool antigen test: repeat post tx for eradication (make sure tx worked)
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15
Q

How is H pylori dx

A

ENDOSCOPY – bx specimen of stomach and duodenum, then RAPID UREASE TEST (pH indicator changes color if urease PRESENT)

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16
Q

How are ulcers dx

A

Either UGI or EGD

  • UGI with barium for contrast, with air and barium for double contast (use Gastrografin if suspected perf) shows location, maybe filling defect or extension beyond lumen, radiating folds extending to ulcer margin [follow up with EGD]
  • UGI not as effective for detecting ulcers <.5cm, and can’t do biopsy
  • PREFER EGD IS AVAILABLE to dx PUD esp with gastric ulcers
17
Q

What are the dx and therapeutic indications for EGD

A

Dx: define site of defect seen on UGI, tissue bx, folloup treated ulcers exp gastric (6wk), eval dyspagia, dyspepsia, abdominal pain

Therapeutic: remove FB, polyp; Sclerosis or banding or esophageal varices; coagulation

18
Q

What are the different pharm tx options for pUD

A
  1. antacids (not very reliable/fast healing)
  2. H2 receptor antagonists
  3. PPI ***
  4. Cytoprotectants (sucralfate)
  5. PG analogs (misoprostol aka cytotec)
  6. Prokinetics (reglan (metoclopromide))
  7. Antimicrobial agents
19
Q

What antacids are available and what is their purpose

A
  • before meal or bedtime can help heal minor ulcers with min SE
    1. Aluminum hydroxide (Maalox) – Constipation
    2. Mg salts (Gaviscon) – Diarrhea
20
Q

What are the H2 Receptor blockers, how do they work

A

Competitively inhibit histamine at H2 recptor of gastric parietal cells
Reduce gastric acid secretion, gastric secretory volume and hydrogen concentration
Promote healing of DUODENAL ULCER (almost all w/in 8wk)
SAFE! (cimentidine may level of warfarin, theophylline, phenytoin, TCA, quinidine)
BID or QHS dose; proportional to nocturnal acid secretion, so PREFER SINGLE NIGHT DOSE

  1. Tagamet (cimetidine)
  2. Zantac (Ranitidine)
  3. Pepcid (famotidine)
  4. Axid (Nizatidine)
21
Q

How do PPIs work and how should they be used?

A

“prazoles” (prilosex, protonix, prevacid)
Mainstay tx for PEPTIC ULCERS (better than H2RA)
Most powerful inhibitors of GASTRIC acid secretion (DOC for tx of ZES)
Inhibit H/K ATPase proton pump
Effective when parietal cell is stimulated to secrete acid in response to a meal
Should only be taken before a meal, do not use with H2RA or antisecretory agents

22
Q

How does the cytoprotectant Sucralfate help PUD

A

Sucralfate
no direct effect on gastric acid secretion
Forms viscous adhesive substance that protects GI lining against pepsin, peptic acid and bile salts; TAKE ON EMPTY STOMACH
PUD >1 g po QID
Preventing duodenal ulcer relapse: 1 g BID

23
Q

How do PG analogs work

A

Protect gastroduodenal mucosa
Stimulate secretion of bicarb and mucus, good for prevention of NSAID induced ulcers
Enhance mucosal blood flow; antisecretory effect when given at high doses
Misoprostol (CYTOTEC)2-4x/d
Poor compliance, greater SE: HA, abd pain, diarrhea

24
Q

How should you treat NSAID induced ulcers

A
  1. Elim or reduce NSAIDS, add H2RA
    OR
  2. PPI (PREFER)
25
Q

What are assoc complications of PUD

A

Perf, Hemorrhage, obstruction, intractability, or intolerant of meds

26
Q

S/sx of ulcer perforation

A
  • most common: ACUTE ONSET OF SEVERE ABD PAIN
  • worst in epigastrium, may radiate to lower quadrants or be referred to the shoulders due to diaphragmatic irritation, NV
  • 10-15% present with hemorrhage
27
Q

PE findings associated with ulcer perf? Tx?

A

No or low fever
Tachycardia, Tachypnea
Tender abdomen with signs of peritonitis (guarding, rebound tenderness or rigidity)
*absent BS
*free air (pneumoperitoneum) under diaphragm on plain film (upright CXR) “double wall” sign; if pt unable to stand, use lateral decubitus
TX = surgery

28
Q

How is hemorrhage associated to PUD and what are the s/sx/tx

A

Erosion of ulcer into vessel can cause upper GI bleed

  • Sx: syncope, tachycardia, HYPOTN, N and hematemesis (gross blood v coffee grounds)
  • frank blood or maroon colored stool = precipitous bleeding
  • if associated with perf, will see signs of peritonitis (guarding, rebound tenderness)
  • VOLUME REPLACEMENT, gastric lavage, IV H2RA or PPI (pref) and EMERGENT EGD
  • if unable to control bleeding via EGD, need surgical repair
29
Q

What is Gastric outlet obstruction, how is it related to PUD, and what are s/sx/PE

A

PUD most common cause of gastric outlet obstruction

  • chronic mid epigastric pain, N, persistent vomiting after eating, bloating, sense of fullness in epigastrium and wt loss
  • abdominal distension and succussion splash over epigastrium while abdomen is shaken from side to side

tx: REFER TO SURGEON (gastrectomy with gastro duodenal or gastro jejunal anstomosis; or antrectomy with truncal vagotomy)

30
Q

What are complications assoc with surgery for gastric outlet obstruction

A
  1. Dumping syndrome – acute onset anxiety, weakness, tachycardia, diaphoresis, palpitations after meal with high osmolarity
  2. Blind loop syndrome (seen with BII) – overgrowth of bacteria interferes w/ folate and B12 absorption
  3. Afferent Loop syndrome (seen with BII) – distension from retention of pancreatic and biliary secretions
31
Q

What is ZES and what is it associated with

A

Zollinger Ellison syndrome: gastrinoma, non beta islet cell tumor of the pancreas or paraduodenal area
*excess gastric acid secretion and refractory PUD (ulcers usually in duodenal bulb)
*60% malignant, 50% die w/in 5 yr
SUSPECT IF + FH or PUD or endocrine dz (associated with Mult endocrin Neoplasia (MEN) syndrome)

32
Q

How do pt with ZES present

A

Abdominal pain, severe reflux esophagitis, diarrhea (due to large volume of acidic fluid that flows from stomach into SI) and steatorrhea (from acid hypersecretion, inactivation of pancreatic lipase)

33
Q

Tx of ZES

A

Fasting serum gastrin level for presence of ZES if suspected
*(Levels >300)
May check gastrin after secretin infusioln
*increase >200 over baseline

  • PPIs are DOC, continue as long as needed
  • may need surg resection of tumor
34
Q

90-95% of Gastric cancers are what? And when/who?

A

90-95% are adenocarcinomas
Rarely before 40yo
Men higher risk

35
Q

Causes of Gastric cancer

A 
H pylori (if not treated)
Chronic gastritis
Gastric polyps
Previous gastric surgery
Genetics: 1st deg relative of pt with gastric CA have 2-3x risk
Seen in pt with FAP and nonpolyposis CRC
36
Q

How do pt with gastric cancer presnt/ signs of mets

A
  • Asymp early or sx attributed to PUD
  • pt start on H2RA or PPI which delayed dx
  • abdominal pain – Mass effect no common hearburn
  • wt Loss, occult GI blood loss w or w/o IDA

Mets: VIRCHOWS node (mets spread to left supraclavicular node) or Sister Mary Josephs node (mets to periumbilical nodes)

37
Q

Presenting sx gastric ca

A

Wt loss, abd pain, nausea, dysphagia, melena, early satiety, ulcer type pain

38
Q

Dx approach to Gastric ca

A

UGI shows path (fixed deformity on UGI, but need EGD for tissue bx

  • CT scan of abd to determine respectability and lymph node involvement
  • gastric CA mets directly or via blood to regional lymph nodes, omentum and liver
39
Q

Gastric ca dx/tx/prognosis

A

After dx, staging to optimize tx plan/prognosis
*CXR, CT, MRI to look for local invasion and/or mets
Tx = surgery (sub-total gastrectomy)
*may f/u with chemo ro radiation; for unresectable tumors provide palliative care

Clin Med III (5 decks)

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